An Overview of Chronic Myeloid Leukemia Treatment: From Tyrosine Kinase Inhibitors to Novel and Emerging Therapies

The Philadelphia chromosome and its linked BCR-ABL1 fusion gene, which causes aberrant tyrosine kinase activity, make chronic myeloid leukemia (CML) a model for molecularly targeted cancer treatment. Although the yearly incidence in the United States remains steady at approximately 2 per 100 000 people, the advent of tyrosine kinase inhibitors (TKIs) has significantly altered the disease landscape. TKIs have greatly improved patient outcomes and reframed CML as a chronic, treatable illness. Nevertheless, the healthcare industry has to come up with new ways to improve patient adherence, reduce side effects, and get past medication resistance. The pathophysiology of CML and the development of TKI-based treatments, including first-, second-, and third-generation medicines, are thoroughly examined in this study. We also focus on the side effect profiles, comparative clinical efficacy, and mechanisms of action, with a focus on patient-centered treatment choices. We also discuss the critical evaluation of the intricacy of TKI resistance, intolerance, and the objective of treatment-free remission. Additionally, the development of new therapeutic approaches is examined as a forward-looking tactic to produce more profound and long-lasting molecular responses which include immune-based therapies, combinatorial approaches, and promising third-generation TKIs. This review aims to improve patient outcomes and identify future avenues in CML research by combining new information with existing knowledge.